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5. HDS Neuro Psych > Strokes > Flashcards

Strokes Flashcards

1
Q

Ischemic Stroke

Definition

A

The sudden death of brain cells in a localized area due to inadequate blood flow.

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2
Q

Stroke

Diagnosis

A
  • Pathological dx defined by irreversible ischemic damage to the brain ⇒ cerebral infarction
  • MRI immediately positive on DWI (93% of the time)
  • ⊕ on CT within 24-48 hours
  • ⊖ MRI/CT does not r/o stroke ⇒ if strong suspicion of infarct based on clinical findings can dx stroke
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3
Q

Stroke

Epidemiology

A
  • #2 killer in the world, #3 in USA
  • #1 disabling illness worldwide
  • Stroke kills almost 130k Americans each year
  • Every year, > 795k people in the US have a stroke
  • Recovery is fraught with complications such as aspiration pneumonias and a variety of other infections, DVT and clinical depression
  • Rehab while helpful rarely restores a person to his prior functioning and even less often the ability to return to work
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4
Q

Stroke Subtypes

A
  • Large vessel thrombotic:
    • Thromboocclusive
    • Thromboembolic
  • Small vessel thrombotic ⇒ Lacunar
  • Cardioembolic
  • Watershed
  • Venous thrombosis
  • Transient ischemic attack (TIA)
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5
Q

Large Vessel Thrombotic Stroke

Mechanisms

A
  • Atherosclerotic
    • Large vessel atheroma with fibrous cap ruptures ⇒ plaque hemorrhage ⇒ exposes collagen and cholesterol to the lumen ⇒ promotes platelet aggregation and thrombosis
    • Older patients
  • Dissection
    • Occurs mostly in the carotid or vertebral arteries
    • Abnormal elastin and collagen in media ⇒ allows blood to dissect ⇒ narrowing of lumen ⇒ slow sluggish flow ⇒ clot formation
    • Consider in younger patients
    • Risk factors: Marfan’s, Ehlers Danlos, hx of trauma

Can involve any of these vessels or their branches.

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6
Q

Large Vessel Thrombotic Strokes

Subtypes

A

2 types of thrombotic stroke:

  • Thrombo-occlusive: clot occludes flow
    • Clot completely occludes the diseased vessel then coagulated blood extends all the way up into the brain
    • Generally, a large stroke in the distribution of that large vessel: carotid or vertebral
    • Often preceded by TIA’s with very similar deficits each time that “crescendo” in severity and duration with each TIA
  • Thromboembolic: artery to artery embolism
    • Near occlusion of the parent vessel results in clot formation over the atheroma or dissection
    • Partial flow ⇒ clot enlargement ⇒ can break off and travel downstream where it lodges in a branch
    • Ex: internal carotid → middle cerebral artery or vertebral artery → posterior cerebral artery
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7
Q

Stroke Severity

A
  • Size of the infarct also determined by adequacy of the collaterals
  • Collateral flow ⇒ other vessels that also contribute flow to that region
  • Older patients with diffuse atherosclerotic disease have poorer collaterals and bigger strokes
  • Younger patients with the same clot may have milder deficits
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8
Q

Carotid Artery Disease

Overview

A
  • Carotid atheroma responsible for most anterior circulation large vessel thrombotic strokes
  • Most disease is in the carotid bifurcation in the neck
  • Mostly atherosclerotic in older and dissection in young
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9
Q

Carotid Artery Disease

Symptomatic Stenosis

A
  • Motor or sensory TIA or stroke appropriate to the ipsilateral carotid
  • Transient monocular blindness (amaurosis fugax) appropriate to the ipsilateral carotid
    • Shade-like loss of vision
    • Caused by arterial embolism from carotid → central retinal artery
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10
Q

Carotid Artery Disease

Management

A
  • Treatment: aggressive medical management
    • Treatment of lipids and HTN
    • Antiplatelet therapy: aspirin, clopidogrel (Plavix), aspirin plus dipyridamole (Persantine) ⇒ nucleoside transport inhibitor and PDE3 inhibitor that inhibits blood clot formation
  • If symptomatic and stenosis > 60% or an ulcerated plaque ⇒ can do endarterectomy or stent (NASCET criteria)
  • Asymptomatic stenosis > 80% ⇒ endarterectomy or stent (ACAS criteria)
  • Endarterectomy ⇒ remove the diseased lining and let the artery form a new endothelium
  • Stent ⇒ inflate a balloon that leaves a metal mesh that compresses the atheroma and allows re-establishment of blood flow
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11
Q

Vertebral Artery Disease

A

Vertebrobasilar disease accounts for 10% of posterior circulation large vessel thrombotic strokes.

  • Atherosclerosis in the older patient or dissection in the young
  • Also thrombotic
  • Treated same as carotid with aggressive medical management and antithrombotic therapy
  • Unlike the carotid, there are no invasive options such as endarterectomy (inaccessible) or stenting (dangerous and ineffective)
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12
Q

Aortic Arch

Thromboembolic Stroke

A
  • 10% of all thromboembolic strokes
  • Seen best with transesophageal echo (TEE)
  • Usually atherosclerotic
  • Tx: maximal medical therapy like for carotid
  • No stenting or surgery
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13
Q

Intracranial Atherosclerosis

A
  • Atherosclerosis of the brain arteries causes thrombotic strokes
  • Presents with recurrent stereotypical TIAs with increasing deficits: crescendo TIA’s culminating in stroke
  • Treatment is maximal medical therapy
  • Rarely reopen artery with endovascular treatment: angioplasty or WINGSPAN-stent
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14
Q

Intracranial Stenosis

Other Etiologies

A
  • Moya-moya
    • Rare in US; seen more in Asia
    • Vasculitis of the major cerebral arteries
    • Collaterals open up and have appearance of puff of smoke on angiogram “moya moya” in Japanese
    • Can be secondary to sickle cell
  • Vasculitis, granulomatous arteritis, fibromuscular dysplasia ⇒ rare causes of intracranial stenosis
  • Infectious arteritis: TB, CMV, syphilis, Herpes zoster in immunocompromised
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15
Q

Lacunar Infarcts

A
  • Small vessel thrombotic strokes and chronic white matter ischemia
  • Each major cerebral vessel → superficial cortical branch & deep branches
  • Small deep vessels supply the deep white matter including internal capsule, thalamus, basal ganglia and pons
  • Small perforating vessels close off ⇒ thrombotic small vessel disease and occlusion
  • When a single deep branch occludes ⇒ very small part of brain is infracted called a lacune (“little lake”) ⇒ limited deficits
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16
Q

Lacunar Syndromes

A
  • The lacunar syndromes include:
    • Pure sensory stroke (involves part of the thalamus)
    • Clumsy hand dysarthria (involves part of the internal capsule)
    • Ataxic hemiparesis
  • When multiple and bilateral, esp. involving white matter corticobulbar tracts ⇒ pseudobulbar affect: inappropriate laughing and crying
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17
Q

Lacunar Infarcts

Pathogenesis

A
  • Lipohyalinosis
    • Progressive thickening of the intima and eventual closure of the lumen of the small perforating arteries ⇒ lacunar infarcts
    • Major cause is HTN
    • Lipohyalinosis can also cause the same vessels to rupture ⇒ ICH
  • Some lacunes are due to atherosclerosis of the ostia of the small penetrating arteries
    • More likely to involve multiple adjacent small arteries
    • Larger lacunes ⇒ “lagoonar infarcts”
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18
Q

Small Vessel Disease

Radiologic Changes

A
  • Can cause white matter changes on MRI and CT called leukoaraiosis
  • Common MRI reading is “evidence of white matter disease / subclinical ischemia”
  • When moderate, a normal finding in older patients especially with migraine and HTN history
    • Causes unnecessary alarm to patients when they read these reports
  • When extensive, can result in cognitive impairment or even vascular dementia
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19
Q

Small Vessel Disease

Treatment

A
  • Treat risk factors
    • Esp. HTN, DM
  • Antiplatelet therapy
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20
Q

Cardio-embolic Strokes

Characteristics

A
  • Atrial fibrillation most common cause
    • Accounts for ~ 15% of strokes in the US
    • ↑ Frequency of A. Fib as more Americans survive to 9th decade
    • Most clots form in the left atrial appendage ⇒ “left atrial cardiomyopathy”
  • Certain features suggest cardioembolic stroke:
    • Sudden onset, can be large
    • Wedge-shaped cortical infarcts
    • Acute strokes involving anterior and posterior circulation or right and left hemispheres simultaneously
    • Strokes in posterior circulation and cerebellum
    • Stroke in language areas with aphasia
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21
Q

Cryptogenic Stroke

A

A brain infarction not clearly attributable to a definite cardio-embolism, large artery atherosclerosis, or small artery disease despite extensive investigation.

Often from A. Fib.

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22
Q

Atrial Fibrillation

Evaluation

A
  • Prolonged cardiac monitoring: loop recorder
  • 2D echo
    • TEE
    • Better imaging of LA appendage
    • Certain patterns suggest embolic source in LAA
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23
Q

Atrial Fibrillation Related Stroke

Treatment

A
  • Oral anticoagulation
    • Warfarin had been the pharmacologic standard for stroke risk reduction in pts with A. Fib
    • Novel oral anticoagulants ⇒ equally effective w/ fewer ICH ⇒ now tx of choice
    • Dabigatran, rivaroxaban, apixaban, edoxaban
  • A. Fib w/o hx of stroke management ⇒ anticoagulation based on CHADS2vasc score
    • Elderly w/ a gait disorder is not a contraindication for anticoagulation
    • Need to fall 800 times to exceed risk of harm from single stroke
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24
Q

Cardiogenic Strokes

Other Etiologies

A
  • Acute MI with dyskinetic segment ⇒ mural thrombus
  • Rheumatic heart disease and mechanical valve replacement
  • SBE (subacute bacterial endocarditis) ⇒ vegetations ⇒ septic emboli to brain ⇒ infarct (often hemorrhagic)
  • Left atrial myxoma ⇒ tumor fragments and travels distally
  • SLE ⇒ Libman Sachs endocarditis
  • Cancer: hypercoagulable state with marantic endocarditis and emboli
  • Severe CHF
  • Cardiac bypass pump during CABG
  • Patent foramen ovale (PFO)
  • Fat embolism ⇒ after long bone fracture
  • Air embolism ⇒ accidentally infusing air into venous or arterial circulation or decompression sickness in diver
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25
Q

Patent Foramen Ovale (PFO)

Related Stroke

A
  • Consider in young person with no classic risk factors: HTN, DM, HLD
  • Paradoxical embolism from venous clot across the PFO
  • Often thrombophilia as well: factor V Leiden, prothrombin gene mutation 20210A, protein S, protein C, antithrombin-3
  • Can be closed but controversial tx
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26
Q

Watershed Infarcts

A
  • Infarction caused by decreased blood flow
  • Most distal vessels first to lose perfusion
  • Combo of large vessel stenosis (carotid, vertebral), upstream stenosis, heart failure (low CO), and poor collaterals
  • Post cardiac arrest: no flow to the brain for minutes, the watershed zones are infarcted first
  • Locations:
    • Cortical border zone infarcts
      • Between 2 vessels both with low flow
        • ACA-MCA ⇒ trunk weakness
        • MCA-PCA ⇒ if b/l prosopagnosia
    • Internal border zone infarcts
      • Between superficial and deep vessels off a major artery
        • MCA-lenticulostriates
        • PCA-thalamoperforators
        • ACA-Huebner’s
  • String of pearls on MRI
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27
Q

Cortical Venous Infarcts

Overview

A
  • Hemorrhagic infarcts due to partial or complete venous sinus or cortical vein thrombosis
  • Not typical distribution of arterial infarcts ⇒ can be B/L or cross expected arterial boundaries
  • See unusual pattern of deficits:
    • Saggital sinus thrombus ⇒ bilateral weakness
    • More seizures
    • Papilledema
    • Headache
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28
Q

Cortical Venous Infarcts

Pathophysiology

A
  • Combo of edema and ischemia:
    • Blood cannot drain into sinus ⇒ back pressure into thin-walled veins ⇒ extravasation of RBCs along with infarction
  • Hemorrhagic conversion common
  • Especially irritating for the brain ⇒ more likely to induce seizures
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29
Q

Venous Thrombosis

Risk Factors

A
  • Post-partum
  • Chemotherapy
  • Underlying infection, inflammation, or malignancy
  • Women on contraceptives
  • Thrombophilia (ex. TPO)
  • Neurosurgery ⇒ meningioma resection (damage the venous sinus)
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30
Q

Cortical Venous Infarcts

Management

A
  • Diagnosis:
    • MRI brain w/gadolinium and MR venography
    • CT brain w/ contrast and CT venography
  • Treatment:
    • Anticoagulation even though may be a hemorrhagic infarct as likely to progress
    • Extreme cases of massive cortical venous sinus thrombosis: continuous tPA infusion into the sinus
    • Look for underlying cause cancer
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31
Q

Transient Ischemic Attack (TIA)

A
  • A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction ⇒ reversible cerebral ischemia
  • Same underlying pathology as stroke but completely reverses
  • Higher risk of a subsequent stroke and if occurs ⅓ will be in the next 48 hours
  • Workup: MRI shows if infarct, image carotids, echo of heart, EKG monitoring for A. Fib
  • Most are admitted
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32
Q

Stroke Presentation

Overview

A
  • Sx depends on which vessel closes
  • Clinical presentation often suggests etiology:
    • Sudden ⇒ embolic
    • Stuttering ⇒ more thrombotic
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33
Q

Brain

Functional Areas

A
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34
Q

Middle Cerebral Artery (MCA)

Complete Occlusion

A

Anterior circulation stroke

  • Frontal and parietal lobes affected:
    • Weakness and sensory loss, arm greater than leg
  • If dominant hemisphere ⇒ aphasia
  • If complete ⇒ life threatening
  • Eyes “looking toward the lesion”
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35
Q

Middle Cerebral Artery (MCA)

Branch Occlusions

A

Anterior circulation stroke

  • Temporo-parietal: Wernicke’s receptive aphasia
  • Frontal: Broca’s expressive aphasia
  • Frontal motor strip: contralateral weakness
  • Parietal sensory strip: contralateral sensory loss
  • Nondominant parietal lobe: hemineglect
  • Dominant parietal lobe: ideomotor apraxia
36
Q

Anterior Cerebral Artery (ACA)

Infarct

A

Anterior circulation stroke

  • Leg greater than arm
  • Rarer because most have intact anterior communicating artery
37
Q

Posterior Circulation Stroke

Overview

A
  • Vertebral artery disease causes posterior circulation stokes
  • Extracranial or intracranial vertebral, basilar and PCA occlusions
  • See various brainstem stroke syndromes
38
Q

Brainstem

Nuclear Columns

A
  • Medial** **⇒** **motor
    • Very medial: somatic motor ⇒ tongue and eye movements
    • Medial: branchiomotor ⇒ facial, jaw, and swallowing and voice muscles
  • Lateral** **⇒** **sensory
    • Lateral: trigeminal nucleus ⇒ ipsilateral facial sensation
    • Far lateral: special sensory ⇒ vestibular nuclei (huge representation in medulla and pons), cochlear nucleus
39
Q

Brainstem

Pathways

A

Also medial ⇒ more motor & lateral ⇒ more sensory

  • Medial:
    • Descending motor: corticospinal tract ⇒ contralateral body weakness (crosses at medullary pyramid)
    • Corticobulbar ⇒ dysarthria
  • Medial/Lateral:
    • Descending sympathetic motor tracts ⇒ pupil, eyelid, facial sweat ⇒ ipsilateral Horner’s syndrome
  • Lateral:
    • Ascending sensory pain and temperature (STT) from contralateral body (crosses in cord) ⇒ contralateral anesthesia body
  • Far lateral:
    • Cerebellar connections (peduncles)
40
Q

Wallenberg Syndrome

Etiology

A
  • Occlusion of the PICA (posterior inferior cerebellar artery)
    • Final branch of the vertebral artery before it joins to form the basilar artery
  • Can be seen with distal vertebral artery occlusion
  • One of the most common brainstem strokes
  • Often misdiagnosed as inner ear disturbance or gastroenteritis
41
Q

Wallenberg Syndrome

Clinical Manifestations

A

Classic brainstem infarct involving the lateral medulla

  • Medial part of lateral medulla ⇒ motor
    • Nucleus ambiguus [motor nucleus of vagus] ⇒ palate and larynx → dysphagia and hoarseness
    • Descending sympathetics ⇒ ipsilateral Horner’s syndrome (ptosis, miosis, anhidrosis)
  • Lateral part ⇒ sensory
    • Descending nucleus/tract of trigeminal ⇒ ipsilateral loss of pain and temperature from face
    • Spinothalamic tract ⇒ contralateral loss of pain and temperature from body
    • Vestibular nuclei ⇒vertigo, N/V, nystagmus
    • Far lateral:
    • Inferior cerebellar peduncle ⇒ ipsilateral ataxia
42
Q

AICA Syndrome

A

Infarct affects lateral caudal pons

  • Similar to Wallenberg syndrome except:
    • Also see tinnitus and hearing loss, facial weakness
    • No motor weakness of swallowing and voice
43
Q

Paramedian Pontine Infarcts

A
  • Lacunar infarcts from small vessel disease of the paramedian pontine perforators
  • Clinically the same as lacunes higher up in internal capsule
  • Motor deficits from corticospinal/ corticobulbar tracts ⇒ limited weakness, dysarthria
44
Q

Hemi-Pontine Infarct

A

Larger territory of unilateral pons infarcted ⇒ “lagoonar infarct”

  • ↑ Corticospinal / corticobulbar tract involvement ⇒ ↑weakness and dysarthria
  • If 6th CN nerve nucleus affected (abducens) ⇒ cannot move the eyes laterally so the eyes drift medially
    • Look away from the lesion ⇒ “wrong way eyes”
      • Vs MCA infarct ⇒ look at the lesion
  • Atherosclerosis of basilar artery knocks off many perforators
  • Ominous as could next occlude the whole basilar artery
45
Q

Basilar Artery Occlusion

A

Total basilar artery occlusion ⇒ total pons infarction

  • Causes Locked In Syndrome
    • Fully awake (reticular activating system spared - is in the midbrain)
    • Quadriplegic except for vertical eye movements and blink
  • Both 6th CN nuclei involved ⇒ no lateral eye movement
46
Q

Top of the Basilar

Syndrome

A

Usually embolic from the vertebral artery or heart

Infarct directly affects midline aspect of midbrain ⇒ Weber Syndrome

  • CN III nuclei ⇒ somatic and parasympathetic motor fibers ⇒ 3rd nerve palsy
    • Ipsilateral lateral strabismus
    • Ptosis
    • Dilated pupil
    • Ophthalmoplegia
    • Loss of accommodation
    • Loss of pupillary reflex
  • Long tract signs:
    • Corticospinal tract ⇒ contralateral spastic hemiparesis
    • Corticobulbar tract ⇒ contralateral lower face weakness​, drooping of the corner of the mouth
  • Leads to clotting into bilateral PCA distributions
    • Occipital lobe ⇒ homonomous hemianopsia (loss of the same half of vision in both eyes)
    • Temporal lobe (hippocampus) ⇒ anterograde amnesia (cannot learn new info)
47
Q

Total Basilar Artery Occlusion

Warning Signs

A

Occlusion/infarct usually due to atherosclerosis ⇒ preceded by crescendo TIAs

  • Vertigo can be peripheral but can also be due to ischemia to the vestibular nuclei
  • Hemiparesis/bilateral leg weakness or dysarthria ⇒ corticospinal and corticobulbar tracts
  • Ataxia: ⇒ cerebellar peduncle/ cerebellum
  • Numbness ⇒ 5th nerve nucleus, spinothalamic, lemniscus tracts
  • Nystagmus ⇒ non-fatiguing, up-beating
  • Diplopia or gaze deviation ⇒ 6th nerve nucleus, lateral gaze center
  • LOC ⇒ lower midbrain RAS (reticular activating)
48
Q

Posterior Circulation Stroke

Warning Signs Mnemonic

A

6 Dangerous D’s and 3 Nasty N’s

  • 6 Dangerous D’s:
    • Dizziness (spinning feeling = vertigo)
    • Dysphagia (problem swallowing)
    • Dystaxia (unsteady w/ walking or coordination problems w/ limbs)
    • Diplopia (double vision)
    • Dysarthria (slurred speech)
    • Drop attacks (sudden loss of power in the legs with falling)
  • 3 Nasty N’s
    • Nausea
    • Numbness (any part of the body)
    • Nystagmus (jerky vision)
49
Q

Acute Ischemic Stroke

Management

A
  • ± Admin of tPA
  • Lower BP only to acceptable range for IV tPA tx: systolic < 185, diastolic < 110
  • Consider thrombectomy and transfer to comprehensive stroke center ⇒ “drip and ship”
    • Large clots that IV tPA cannot reach
    • Hyperdense MCA sign on CT
    • Does not exclude patient from tPA or thrombectomy
    • Recent trials show that stent retrievers used early better long-term outcomes
  • Admission to a stroke unit
  • PT and begin regular exercise as tolerated
  • Reintegration into community
50
Q

Tissue Plasminogen Activator (tPA)

Overview

A

“Clot buster” drug

  • Given within 3-hour window of first signs of stroke
    • Can give at 4.5 hours in select pts with some exclusions
  • Careful selection to avoid hemorrhagic conversion: 2.7% risk
    • 100 patients: 16 benefit, 2.7 harm, the rest no difference
  • Tx goals:
    • Recanalize blocked artery
    • Preserve the ischemic penumbra
51
Q

Tissue Plasminogen Activator (tPA)

Treatment Criteria

A

Careful selection needed to avoid hemorrhagic transformation ⇒ ↑ morbidity and mortality

Preserve ischemic penumbra w/o causing infarct core to bleed

  • Inclusion criteria for tPA:
    • Any clot based arterial ischemic stroke
    • Large vessel thrombotic
    • Small vessel lacunar
    • Cardioembolic
  • Exclusion criteria for tPA:
    • On warfarin and PT INR > 1.6
    • Use of novel oral anticoagulants (NOACs) within 48 hours
    • Major recent surgery
    • Out of the time window
    • Early major changes on CT
52
Q

Stroke Admission

A
  • Admission to a stroke unit:
    • Tx for all stroke patients whether or not getting tPA
    • Studies show a 10% reduction in morbidity and mortality
  • Stroke order sets including:
    • Avoid aggressive tx of BP to normal during first 1-2 days to prevent compromise of penumbra unless getting tPA
    • Swallowing evaluation before PO feeds or meds ⇒ avoid aspiration PNA
    • DVT prophylaxis ⇒ heparin or SCD’s
    • Early mobilization, OOB, PT
    • Statin if LDL > 100
    • Cardiac monitoring to look for A. Fib
    • Antiplatelet Rx prior to D/C unless A. Fib and then anticoagulation
53
Q

Stroke

Secondary Prevention

A

Biggest risk for stroke is already having had one

  • Long term BP control and regular follow-up with an internist
  • Tx diabetes
  • Smoking cessation
  • Tx of hyperlipidemia
  • Avoid heavy regular use of alcohol
  • Weight loss and dietary modification
54
Q

Primary Intracerebral Hemorrhage (ICH)

Definition

A

Bleeding in the brain parenchyma due to a ruptured vessel.

Deep vs lobar

55
Q

Secondary Intracerebral Bleed
Definition

A

Hemorrhagic conversion of a lesion as infarct or tumor.

56
Q

Intraventricular Bleed
Definition

A

Rupture of parenchymal bleed into the ventricles generally from hypertensive bleed.

57
Q

Subarachnoid Hemorrhage
Definition

A

Blood in the subarachnoid space generally from ruptured aneurysm or trauma.

58
Q

Subdural Hematoma
Definition

A

Blood in space between the dura and pia/arachnoid from trauma.

59
Q

Epidural Hematoma
Definition

A

Blood between the calvarium and the dura from trauma.

60
Q

Obstructive Hydrocephalus
Definition

A

Blockage of CSF flow due to blood in the ventricular system.

61
Q

Peri-Hematoma Edema
Definition

A

Area surrounding the bleed

62
Q

Intracerebral Hemorrhage (ICH)

Overview

A
  • Common cause of disability and death
    • Estimated annual incidence of 33 people per 100k
  • 5% die before arrival at medical facilities
  • For the majority that survive, overall prognosis is grave:
    • 35% dying within 7 days
    • 50% by 30 days
    • Large bleeds have up to 80% mortality
  • Expansion in first 1-3 days common ⇒ when clinical deterioration occurs
63
Q

Intracerebral Hemorrhage (ICH)

Management

A
  • Early treatment of hemorrhage is important
  • Aggressive tx of elevated BP ⇒ ↓ risk of expansion
    • Do not worry about compromising an ischemic penumbra w/ aggressive BP lowering
    • Peri-hematoma edema is not an ischemic area
64
Q

Deep Hypertensive Parenchymal

Hemorrhages

A
  • The most common and most lethal of bleeds
  • Due to small vessel disease
    • Damage of endothelium by chronic HTN w/ resultant lipohyalinosis
  • Same vessels and pathologic process of lacunes and same distribution
    • Small perforating arteries to deep structures
    • Basal ganglia, internal capsule, thalamus and pons
  • Instead of the occlusion that causes lacunar infarcts, there is vessel rupture causing deep bleeds
65
Q

Deep Hypertensive Parenchymal Hemorrhages

Management

A
  • Surgical removal of deep bleeds not beneficial
  • Medical management of increased intracranial pressure
    • Osmotic agents to pull fluid out
    • Hypertonic saline
    • Mannitol
    • NOT corticosteroids
      • Useless in cytotoxic edema
      • Useful in vasogenic from brain tumors
    • Endoscopic infusion of tPA into clots may help
66
Q

Deep Parenchymal ICH

Complications

A
  • Cerebral herniation
  • Obstructive hydrocephalus when ventricular extension
    • Drains often ineffective
      • Clot off
    • Blood in ventricle a poor prognostic sign
67
Q

Deep Parenchymal ICH

Outcomes

A
  • Most important prognostic variable ⇒ level of medical support provided
    • Withdrawal of support in pts felt likely to have a poor outcome leads to self-fulfilling prophecies
    • Individual patients in traditionally “poor outcome” categories can have a reasonable neurologic outcome when treated aggressively
  • Very poor prognosis ⇒ survival might be vegetative ⇒ therapeutic nihilism ⇒ affects outcomes
  • AHA guidelines ⇒ No DNR in first 48 hours unless advance directive for such
68
Q

Lobar Hematomas

Overview

A
  • More superficial bleeds, somewhat better prognosis
  • Most often due to cerebral amyloid angiopathy (CAA) or contusion
  • DDx: AVM’s, aneurysm, hemorrhagic transformation of infarct/tumor
  • Often amenable to surgical removal if mass effect and incipient herniation
    • Especially when in cerebellum ⇒ temporal lobe near surface and accessible
69
Q

Cerebral Amyloid Angiopathy

(CAA)

A

Widespread deposition of beta amyloid in the small caliber vessels of brain making them more likely to rupture.

  • Amyloid in vessel walls ⇒ ↑ fragility and liable to rupture
    • More superficial vessels
  • Older patients often have coexisting Alzheimer’s
    • Same amyloid in vessels as in brain parenchyma ⇒ Amyloid neuritic plaques
    • Alzheimer’s not an absolute contraindication for lifesaving superficial clot evacuation
  • Microbleeds
    • Macro-bleeds often in site of prior microbleed
    • Presence may increase risk of anticoagulation related bleeds
    • Exact risk not known
70
Q

Anticoagulation-related

Hemorrhage

A
  • From warfarin used for A. Fib, DVT and prosthetic cardiac valves or novel anticoagulant (NOAC) used for A. Fib, DVT
    • Warfarin reversible w/ vitamin K dependent factors as it antagonizes these
    • NOACs less easily reversed
    • Only dabigatran has an antidote
  • Timing of restarting anticoagulation especially w/ prosthetic heart valves tricky
    • Restart too early and extend bleed
    • Wait too long and re-stroke
71
Q

Hemorrhagic Conversions

A
  • Post tPA
    • More when protocol violations
    • Treating over 4.5 hours
    • Treat supportively like any bleed
    • No agreed upon reversal agent
  • Embolic strokes tend to be hemorrhagic
    • Abrupt cut off of flow, ischemic endothelium then partial reestablishment of flow
    • RBC extravasation and hemorrhagic conversion
    • More when large stroke
  • In A. Fib, wait a week to anti-coagulate to prevent conversion
  • Hemorrhagic conversion of primary brain tumor as glioblastoma or metastasis as melanoma or renal cell CA
  • Both vascular tumors
  • Hemorrhagic conversion of cortical venous infarcts
72
Q

Hemorrhagic Conversion

Arterial Stroke

A
  • Often embolic and large infarct
    • Ischemia of the vascular endothelium then re-establish flow
    • Can be post tPA
      • More when protocol violations
      • Supportive Tx, reversal???
  • Prevention
    • In large stroke from A. Fib, wait 1 week to begin anticoagulation
73
Q

Hemorrhagic Conversion

Cortical Venous Infarct

A
  • Back pressure from obstructed venous drainage ⇒ extravasation of RBCs ⇒ hemorrhagic infarct
  • If due to sinus thrombosis, need to anti-coagulate ⇒ ↑ bleeding risk
74
Q

Hemorrhagic Conversion of Tumors

A
  • Primary
    • Glioblastoma multiforme (GBM)
    • Very vascular and necrotic so often bleeds
  • Metastatic
    • Especially melanoma, renal cell which are very vascular
  • Treat w/ corticosteroids for vasogenic edema
75
Q

Cerebral Aneurysm Rupture

Overview

A
  • Mostly in Circle of Willis
    • Most rupture into peri-chiasmatic cistern ⇒ subarachnoid hemorrhage
    • Rarely aneurysm rupture aims into the brain ⇒ parenchymal bleed
  • Re-rupture common
  • Day 3-5 vasospasm common
    • Multiple strokes and high mortality
    • Need early clipping or coiling of aneurysm (day 1-2) so hypervolemic/hypertensive therapy can be given without re-rupture before vasospasm sets in
  • At first may not see aneurysm on angiogram because of arterial spasm
    • Must repeat angiogram later
76
Q

Cerebral Aneurysm Rupture

Locations

A

3 most common locations to rupture:

Anterior Communicator (ACOM)

Middle Cerebral Artery (MCA)

Posterior Communicator (PCOM)

77
Q

Anterior Communicator (ACOM)

Rupture

A
  • Most common to rupture (40%)
  • Adjacent to optic chiasm and mesial basal frontal lobe so neighborhood signs of:
    • Visual field defects such as bitemporal heteronymous hemianopsia
      • Due to compression of the optic chiasm
    • Frontal lobe pathology
    • Change in personality
78
Q

Middle Cerebral Artery (MCA)

Rupture

A
  • 2nd most common aneurysm to rupture (34%)
  • Deep in temporal lobe
  • Can present as a space occupying lesion causing temporal lobe seizures
  • Can look like brain tumor and attempts at resection = disaster
79
Q

Posterior Communicator (PCOM)

Rupture

A
  • 3rd most common site to rupture (20%)
  • Runs over the exiting 3’d nerve so neighborhood signs of:
  • Compressed 3’d nerve w/ blown pupil and ptosis and sparing eye movements
    • “Surgical 3’d”
80
Q

Aneurysm Rupture

Risk Factors

A
  • Size over 10 mm
    • Under 3mm very unlikely to rupture
  • Smoking
  • Continued hypertension
  • More in polycystic kidney disease and Marfan syndrome, Ehlers Danlos syndrome
  • Genetics
    • If two 1st degree family members w/ aneurysm, rest should be screened
    • Consider coiling if unruptured
81
Q

Migraine vs Aneurysm

A
  • Sometimes warning leak from an aneurysm causes “sentinel headache”
  • Suspect if: worst headache of one’s life, sudden-onset, stiff neck, wakes from sleep
  • Imaging: CT picks up vast majority of SAH
    • L/P at discretion of MD
  • The current consensus is that structural changes in the aneurysm wall or minor bleeding could be the factors responsible for the pain
82
Q

Arteriovenous Malformations (AVM)

A

Direct connection of artery to vein without arterioles or capillaries intervening

  • Arterial BP against thin-walled veins
    • Result is tendency to catastrophic bleed
  • Extension of AVM to form many interconnected branches
    • Difficult to tie off all of them
    • Like “cutting the head off a medusa
    • Cut one and 3 more pop-up”
  • Treatment: Embolize first to close as many branches and feeder vessels prior to surgical excision
83
Q

Cavernous Hemangioma

(Cavernoma)

A
  • Small malformed veins, low pressure and slow flow
  • Often leak but not life-threatening
    • Causes local neurologic dysfunction that gradually clears
      • E.g. brainstem location might cause dysarthria
  • Without imaging, can behave like ischemic stroke or multiple sclerosis plaque
  • Often misdiagnosed as either
  • No specific tx and prognosis favorable
  • Can be multiple, often familial
84
Q

Cerebral Contusions

A
  • Coup lesions
    • Direct force on brain at point of impact
  • Contrecoup
    • Brain trauma on opposite side of head to direct trauma as result of brain moving through CSF and slamming into the calvarium
  • Clues that it is traumatic: soft tissue swelling on exam and CT
  • Frontal and temporal bones most common
  • Increasing cause of cerebral bleeds w/ aging population and frequent falls
85
Q

ICH

Summary

A
  • ICH is a serious disease w/ high morbidity and mortality
  • Despite poor prognosis of large deep bleeds, must treat aggressively within 1st 48 hours
    • Aggressive reduction of BP early standard of care
    • Neurosurgical input vital, mostly for supportive ICU care
    • Ventricular drainage when hydrocephalus, herniation
  • Most common and most lethal bleeds are hypertensive deep hemorrhages
  • Lobar bleeds more superficial, can be amenable to surgical resection especially if incipient herniation
    • Often due to CAA, AVMs, hemorrhagic conversions of infarcts or tumors
  • Saccular aneurysm rupture usually causes SAH
    • Treated w/ clipping early to allow hypertensive/ hypervolemic therapy during the eventual vasospasm at day 3-7
  • Hemorrhagic conversion of arterial infarcts more common when large and embolic and seen w/ IV tPA
  • Hemorrhagic venous infarct should be considered when unusual distribution of infarct not following arterial circulation
    • Consider thrombophilia, either acquired or genetic

5. HDS Neuro Psych (46 decks)

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